纳洛酮对心肺复苏犬脑组织一氧化氮、S100蛋白表达的影响

Changes of nitric oxide and protein S100 by naloxone in postresuscitation dog from cardiac arrest

目的通过检测心跳骤停犬复苏后及给予纳洛酮干预后脑组织中一氧化氮(NO)、S100蛋白表达情况,了解纳洛酮对脑复苏的影响。方法18只健康杂种犬,随机分成三组,每组6只,予体外电击诱发室颤,对照组心跳骤停后予标准心肺复苏术;纳洛酮组心跳骤停后予标准心肺复苏术+纳洛酮;空白组不诱发室颤,于复苏后6h取脑海马组织行脑形态学检查及NO、S100蛋白表达的测定。结果纳洛酮组S100蛋白表达明显低于对照组(P<0.01),对照组脑组织NO的含量高于纳洛酮组(P<0.01),纳洛酮组脑组织的病理损害低于对照组。结论使用纳洛酮后心肺复苏犬脑组织的病理损害有所减轻,脑组织NO、S100蛋白的生成也显著减少,纳洛酮可能通过减少NO、S100蛋白的表达而减轻心肺复苏后脑的再灌注损伤。

Objective To discuss the expression of NO, S100 and the pathological changes of dog＇s cerebral tissue which were actualized CPR, and their effects by naloxone. Methods Eighteen healthy adult cross dogs were separated three groups stochastically （ n = 6）. Blank group were not induced ventricular fibrillation, collected the cerebral tissues after 6 hours. Control group were actualized standard CPR after cardiac arrest. Naloxone group were actualized standard CPR and used naloxone after cardiac arrest. The control group and naloxone group were collected the cerebral tissues after 6 hours when they had been actualized CPR and detected the NO, S100 concentration and pathological changes. Results The concentrations of NO, S100 in control group were higher than those blank group （ P 〈 0.01 ） and naloxone group （ P 〈 0.01 ）. Control group presented obvious pathological damage of nerve cell and the damage of naloxone group was lower than the control group. Conclusion Naloxone can reduce the production of NO, S100 in cerebral tissue and it＇s pathological damage after cardiopulmonary resuscitation （CPR）, and reduce the nerve cellg reperfusion injury.